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Electrophysiological evidence of demyelination in brachial neuritis
60P
Society proceedings
toxin A (BTX-A) helps chronic limb spasticity. We have studied 71 patients, of ages 5-82 years, with moderate to severe spasticity of the upper (26) or lower limbs (48) refractory to treatment. Underlying causes were stroke (31), head injury (1 1), heredofamilial spastic paraparesis (7), multiple sclerosis (7), cerebral palsy (5), Friedreich’s ataxia (4) and other (6). Outcome measures were clinical and blinded videotape assessments of spastic@ and motor function. Electromyographyguided BTX-A injections were given to total doses averaging 175 units in an upper limb (range 2&445 units) and 200 units in a lower limb (range 60-500 units). Forty-three patients (61%) derived marked and 19 patients mild benefit; with improved limb posture and range of passive motion in 54, pain reduction in 46 of 54 with pain, and improved function in 28. Of 32 patients receiving repeat injections, all have had reproducible benefit. Side effects were limited to local discomfort from the injections (40), symptomatic local weakness (2) and local infection (1). In conclusion, preliminary experience indicates that BTX-A is a useful adjunctive treatment for selected patients with spasticity. 5.
Electrophysiological evidence of demyelination in bra&al neuritis. - Mark W. Faragher, Didier P. Cros (Massachusetts General Hospital, Boston, USA)
Brachial neuritis has been traditionally regarded as a predominantly axonal process. Five patients with clinical presentations compatible with brachial neuritis were assessed with nerve conduction studies, cervical root stimulation, needle electrode examination, and somatosensory evoked potentials. The patients showed a combination of electrophysiological findings suggestive of demyelination, including conduction block on cervical root stimulation, markedly prolonged latencies on cervical root stimulation, prolonged F wave latencies, myokymic discharges on needle electrode examination, and prolonged somatosensory evoked potential latencies. These findings have implications regarding the pathogenesis and treatment of some cases of brachial neu-
ritis. 6.
Vestibular projections to limb muscles as revealed by galvanic vestibular stimulation. - Richard Fitzpatrick (Prince of Wales Medical Research Institute, Randwick, NSW)
Galvanic vestibular stimulation can evoke postural sway and transient EMG activity in the leg muscles. Normal adult subjects stood and turned their heads to face over the left shoulder. Impulses of current (0.5-4 mA) were applied between the mastoid processes through large (6-8 cm2) electrodes. Post-stimulus averages of 32 trials were calculated. At a mean latency of 56 ms, there were reciprocal changes in soleus and tibialis anterior muscle activity followed, at 105 ms, by huger responses of opposite sign. Responses were reversed by changing stimulus polarity and by turning the head to the right. Both early and late responses increased with stimulus intensity, but the early response had a higher threshold and was only seen with stimuli above 1 mA. With 2 mA stimuli, soleus EMG was modulated by 20% during the early response and by 40% during the later response. The responses were modified by different postural tasks. When balancing on an unstable platform where there is an increased reliance on vestibular input, responses were larger. No responses were evoked when seated subjects made voluntary contractions of the leg muscles, or when they were supported upright and used the leg muscles to balance a body-like load. When scaled for background EMG levels, there were no changes in the responses with eye closure. The EMG responses produced small transient movements, but were followed at long latency (400 ms) by a large prolonged sway, which was not attributable to the earlier EMG responses. When subjects were supported and movement prevented, the stimuli produced illusory movements in the direction opposite to the sway evoked when standing, as if the prolonged sway was a reaction to the illusion of sway. It is concluded that (i) biphasic EMG responses are produced by galvanic vestibular stimulation,
(ii) the strength of vestibular effects on muscles depends on whether they are required for postural stability, and (iii) if proprioceptive cues are appropriate, visual inputs have little effect on the vestibular rcsponse. 7.
Discharge of human diaphragm motor units during voluntary inspiratory tasks. - S.C. Gandevia, J.E. Butler, J.B. Leeper, D.K. McKenzie (Prince of Wales Medical Research Institute, Randwick,
NSW)
The recruitment and firing characteristics of the human diaphragm motor units were assessed with a monopolar electrode inserted through the right 7th or 8th intercostal space (midaxillary line) into the costal diaphragm. When a single motor unit was identified, subjects (n = 4) followed 8 different time-lung volume ramps in random order. Four tasks involved inspiration to a constant target lung volume (20% vital capacity, VC) at different inspiratory flows (2.5-20% K/s). Four tasks were performed with a constant inspiratory flow (5% VC/s) to different lung volumes (540% VC). Sixty motor units were identified and 47 units were studied in at least 5 or more tasks. There was no evidence of a bimodal distribution of the time of recruitment of motor units. The average recruitment frequency was about 8.4 Hz (IQ range 4.4-lO.OHz) for target tidal breaths and it increased with higher inspiratory flows. Mean firing frequency during inspiration across all tasks was 10.5 Hz (range 8.4 f 0.2 Hz-12.7~1~0.7 Hz). Discharge frequencies increased as both inspiratory flow and volume increased. 8.
Pathophysiology of spa&city. - Jean-Michel Gracies (Prince of Wales Medical Research Institute, Randwick, NSW)
Spastic@ is addressed using its classical definition of a velocitydependent increase in the reflex response to muscle stretch. After a central lesion, damage to descending pathways will alter spinal reactivity that will undergo rearrangements after a variable period of time. This will produce abnormal reflex contractions, some of which meet the classical definition of spasticity. Concomitantly, muscle immobilisation resulting from paresis, and abnormal patterns of contraction, will produce changes in muscle properties which may aggravate spasticity. At the spinal level, the abnormalities causing spasticity may vary according to the site and extent of the lesion. Indirect arguments point toward an increased excitability of a motoneurons but this could not as yet be directly demonstrated. A limited number of microneurographic recordings from Ia afferents failed to find evidence of overactivity of the fusimotor system, and further studies along this line are currently being undertaken. Presynaptic inhibition of Ia terminals has been found to be reduced in paraplegics, while unchanged in hemiplegics. At the muscle level, changes in muscle properties, both active (increased torque/BMG ratio) and passive (reduced extensibility with increasing stretch transmission to spindles), probably contribute to enhance the stretch reflex response. Other spinal abnormalities may have an indirect role in spasticity itself, but could explain other features of the upper motoneuron syndrome. In the lower limb, there is a reduction of reciprocal Ia inhibition on extensors which could be related to an increase in Renshaw inhibition (found at rest in most patients and also during active movement in hemiplegics) and may participate in co-contraction. On flexors, reciprocal Ia inhibition is increased which may play a role in their weakening when antagonists are hyperactive. Non-reciprocal Ib inhibition is decreased, which may account for the common difficulty to stop contraction (slow derecruitment of motor units). Inhibition from small diameter afferents has been found in spastics but it is not known whether it is reduced compared to normals. The extent of disability produced by spastic&y is difficult to assess (it could have an impact in fast concentric movements) but is probably minor in the context of more disabling features caused by the CNS lesion, such as paresis, slowness of motor unit recruitment and derecruitment, muscle shortening and co-contraction.
Society proceedings
toxin A (BTX-A) helps chronic limb spasticity. We have studied 71 patients, of ages 5-82 years, with moderate to severe spasticity of the upper (26) or lower limbs (48) refractory to treatment. Underlying causes were stroke (31), head injury (1 1), heredofamilial spastic paraparesis (7), multiple sclerosis (7), cerebral palsy (5), Friedreich’s ataxia (4) and other (6). Outcome measures were clinical and blinded videotape assessments of spastic@ and motor function. Electromyographyguided BTX-A injections were given to total doses averaging 175 units in an upper limb (range 2&445 units) and 200 units in a lower limb (range 60-500 units). Forty-three patients (61%) derived marked and 19 patients mild benefit; with improved limb posture and range of passive motion in 54, pain reduction in 46 of 54 with pain, and improved function in 28. Of 32 patients receiving repeat injections, all have had reproducible benefit. Side effects were limited to local discomfort from the injections (40), symptomatic local weakness (2) and local infection (1). In conclusion, preliminary experience indicates that BTX-A is a useful adjunctive treatment for selected patients with spasticity. 5.
Electrophysiological evidence of demyelination in bra&al neuritis. - Mark W. Faragher, Didier P. Cros (Massachusetts General Hospital, Boston, USA)
Brachial neuritis has been traditionally regarded as a predominantly axonal process. Five patients with clinical presentations compatible with brachial neuritis were assessed with nerve conduction studies, cervical root stimulation, needle electrode examination, and somatosensory evoked potentials. The patients showed a combination of electrophysiological findings suggestive of demyelination, including conduction block on cervical root stimulation, markedly prolonged latencies on cervical root stimulation, prolonged F wave latencies, myokymic discharges on needle electrode examination, and prolonged somatosensory evoked potential latencies. These findings have implications regarding the pathogenesis and treatment of some cases of brachial neu-
ritis. 6.
Vestibular projections to limb muscles as revealed by galvanic vestibular stimulation. - Richard Fitzpatrick (Prince of Wales Medical Research Institute, Randwick, NSW)
Galvanic vestibular stimulation can evoke postural sway and transient EMG activity in the leg muscles. Normal adult subjects stood and turned their heads to face over the left shoulder. Impulses of current (0.5-4 mA) were applied between the mastoid processes through large (6-8 cm2) electrodes. Post-stimulus averages of 32 trials were calculated. At a mean latency of 56 ms, there were reciprocal changes in soleus and tibialis anterior muscle activity followed, at 105 ms, by huger responses of opposite sign. Responses were reversed by changing stimulus polarity and by turning the head to the right. Both early and late responses increased with stimulus intensity, but the early response had a higher threshold and was only seen with stimuli above 1 mA. With 2 mA stimuli, soleus EMG was modulated by 20% during the early response and by 40% during the later response. The responses were modified by different postural tasks. When balancing on an unstable platform where there is an increased reliance on vestibular input, responses were larger. No responses were evoked when seated subjects made voluntary contractions of the leg muscles, or when they were supported upright and used the leg muscles to balance a body-like load. When scaled for background EMG levels, there were no changes in the responses with eye closure. The EMG responses produced small transient movements, but were followed at long latency (400 ms) by a large prolonged sway, which was not attributable to the earlier EMG responses. When subjects were supported and movement prevented, the stimuli produced illusory movements in the direction opposite to the sway evoked when standing, as if the prolonged sway was a reaction to the illusion of sway. It is concluded that (i) biphasic EMG responses are produced by galvanic vestibular stimulation,
(ii) the strength of vestibular effects on muscles depends on whether they are required for postural stability, and (iii) if proprioceptive cues are appropriate, visual inputs have little effect on the vestibular rcsponse. 7.
Discharge of human diaphragm motor units during voluntary inspiratory tasks. - S.C. Gandevia, J.E. Butler, J.B. Leeper, D.K. McKenzie (Prince of Wales Medical Research Institute, Randwick,
NSW)
The recruitment and firing characteristics of the human diaphragm motor units were assessed with a monopolar electrode inserted through the right 7th or 8th intercostal space (midaxillary line) into the costal diaphragm. When a single motor unit was identified, subjects (n = 4) followed 8 different time-lung volume ramps in random order. Four tasks involved inspiration to a constant target lung volume (20% vital capacity, VC) at different inspiratory flows (2.5-20% K/s). Four tasks were performed with a constant inspiratory flow (5% VC/s) to different lung volumes (540% VC). Sixty motor units were identified and 47 units were studied in at least 5 or more tasks. There was no evidence of a bimodal distribution of the time of recruitment of motor units. The average recruitment frequency was about 8.4 Hz (IQ range 4.4-lO.OHz) for target tidal breaths and it increased with higher inspiratory flows. Mean firing frequency during inspiration across all tasks was 10.5 Hz (range 8.4 f 0.2 Hz-12.7~1~0.7 Hz). Discharge frequencies increased as both inspiratory flow and volume increased. 8.
Pathophysiology of spa&city. - Jean-Michel Gracies (Prince of Wales Medical Research Institute, Randwick, NSW)
Spastic@ is addressed using its classical definition of a velocitydependent increase in the reflex response to muscle stretch. After a central lesion, damage to descending pathways will alter spinal reactivity that will undergo rearrangements after a variable period of time. This will produce abnormal reflex contractions, some of which meet the classical definition of spasticity. Concomitantly, muscle immobilisation resulting from paresis, and abnormal patterns of contraction, will produce changes in muscle properties which may aggravate spasticity. At the spinal level, the abnormalities causing spasticity may vary according to the site and extent of the lesion. Indirect arguments point toward an increased excitability of a motoneurons but this could not as yet be directly demonstrated. A limited number of microneurographic recordings from Ia afferents failed to find evidence of overactivity of the fusimotor system, and further studies along this line are currently being undertaken. Presynaptic inhibition of Ia terminals has been found to be reduced in paraplegics, while unchanged in hemiplegics. At the muscle level, changes in muscle properties, both active (increased torque/BMG ratio) and passive (reduced extensibility with increasing stretch transmission to spindles), probably contribute to enhance the stretch reflex response. Other spinal abnormalities may have an indirect role in spasticity itself, but could explain other features of the upper motoneuron syndrome. In the lower limb, there is a reduction of reciprocal Ia inhibition on extensors which could be related to an increase in Renshaw inhibition (found at rest in most patients and also during active movement in hemiplegics) and may participate in co-contraction. On flexors, reciprocal Ia inhibition is increased which may play a role in their weakening when antagonists are hyperactive. Non-reciprocal Ib inhibition is decreased, which may account for the common difficulty to stop contraction (slow derecruitment of motor units). Inhibition from small diameter afferents has been found in spastics but it is not known whether it is reduced compared to normals. The extent of disability produced by spastic&y is difficult to assess (it could have an impact in fast concentric movements) but is probably minor in the context of more disabling features caused by the CNS lesion, such as paresis, slowness of motor unit recruitment and derecruitment, muscle shortening and co-contraction.